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  • 1
    Electronic Resource
    Electronic Resource
    Osmotically-induced nerve taurine depletion and the compatible osmolyte hypothesis in experimental diabetic neuropathy in the rat (1993)
    Springer
    Diabetologia 36 (1993), S. 608-614 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; experimental neuropathy ; taurine ; osmoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetic neuropathy results from progressive nerve fibre damage with blunted nerve regeneration and repair and may be complicated by nerve hyperexcitability resulting in pain. The naturally occurring amino acid taurine functions as an osmolyte, inhibitory neurotransmitter, and modulator of pain perception. It is also known to have neurotrophic actions. The compatible osmolyte hypothesis proposes that levels of intracellular organic osmolytes including taurine and myo-inositol, respond co-ordinately in response to changes in intracellular sorbitol or external osmolality to maintain the intracellular milieu. We hypothesize that glucose-induced sorbitol accumulation in diabetes mellitus will result in taurine depletion in peripheral nerve which may potentially impair nerve regeneration and precipitate neuronal hyperexcitability and pain. This study explored the relationships of taurine, myo-inositol and sorbitol in the rat nerve and their effects on nerve conduction velocity. Osmolyte levels and nerve conduction velocity were determined in sciatic nerve from non-diabetic and streptozotocin-induced diabetic rats, with or without dietary taurine or myo-inositol supplementation. Taurine levels decreased by 31% (p〈 0.01) and myo-inositol decreased by 37% (p〈0.05) in diabetic nerve as sorbitol accumulated. Taurine supplementation of diabetic animals did not affect nerve conduction velocity but further reduced nerve myo-inositol levels. Prevention of sorbitol accumulation with the aldose reductase inhibitor sorbinil increased nerve taurine levels by 22% (p〈0.05) when compared with untreated diabetic animals. Thus, we have demonstrated an interdependence of organic osmolytes within the nerve. Abnormal accumulation of one osmolyte results in reciprocal depletion of others. Diabetic neuropathy may be an example of maladaptive osmoregulation, nerve damage and instability being aggravated by taurine depletion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404069
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  • 2
    Electronic Resource
    Electronic Resource
    Diabetes-induced changes in lens antioxidant status, glucose utilization and energy metabolism: effect of DL-α-lipoic acid (1998)
    Springer
    Diabetologia 41 (1998), S. 1442-1450 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Lens ; streptozotocin-diabetic rat ; dl-α-lipoic acid ; sorbitol pathway ; redox and energy status
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The study was aimed at evaluating changes in lens antioxidant status, glucose utilization, redox state of free cytosolic NAD(P)-couples and adenine nucleotides in rats with 6-week streptozotocin-induced diabetes, and to assess a possibility of preventing them by dl-α-lipoic acid. Rats were divided into control and diabetic groups treated with and without dl-α-lipoic acid (100 mg · kg body weight–1· day–1, i. p.). The concentrations of glucose, sorbitol, fructose, myo-inositol, oxidized glutathione, glycolytic intermediates, malate, α-glycerophosphate, and adenine nucleotides were assayed in individual lenses spectrofluorometrically by enzymatic methods, reduced glutathione and ascorbate – colorimetrically, and taurine by HPLC. Free cytosolic NAD+:NADH and NADP+:NADPH ratios were calculated from the lactate dehydrogenase and malic enzyme systems. Sorbitol pathway metabolites were found to increase, and antioxidant concentrations were reduced in diabetic rats compared with controls. The profile of glycolytic intermediates (increase in glucose 6-phosphate and fructose 6-phosphate, decrease in fructose1,6-diphosphate, increase in dihydroxyacetone phosphate, 3-phosphoglycerate, phosphoenolpyruvate, pyruvate, and no change in lactate), and 5.9-fold increase in α-glycerophosphate suggest diabetes-induced inhibition of glycolysis. Free cytosolic NAD+:NADH ratios, ATP levels, ATP/ADP × inorganic phosphate (Pi), and adenylate charge were reduced in diabetic rats while free cytosolic NADP+:NADPH ratios were elevated. Diabetes-induced changes in the concentrations of antioxidants, key glycolytic intermediates, free cytosolic NAD+:NADH ratios, and energy status were partially prevented by dl-α-lipoic acid, while sorbitol pathway metabolites and free cytosolic NADP+:NADPH ratios remained unaffected. In conclusion, diabetes-induced impairment of lens antioxidative defense, glucose intermediary metabolism via glycolysis, energy status and redox changes are partially prevented by dl-α-lipoic acid. The findings support the important role of oxidative stress in lens metabolic imbalances in diabetes. [Diabetologia (1998) 41: 1442–1450]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051090
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  • 3
    Electronic Resource
    Electronic Resource
    Selective neuropathy and preserved vascular responses in the diabetic Charcot foot (1992)
    Springer
    Diabetologia 35 (1992), S. 148-154 
    Details
    ISSN: 1432-0428
    Keywords: Charcot arthropathy ; selective neuropathy ; blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Charcot arthropathy is a disabling complication of diabetic neuropathy. It is however, unclear why it occurs in only a small number of neuropathic patients. We have studied 12 diabetic patients (10 insulin-dependent) with an acute Charcot arthropathy, and compared their neuropathy and vascular responsiveness with 12 diabetic patients (10 insulin-dependent) with recurrent neuropathic foot ulceration, 12 diabetic control subjects (9 insulin-dependent) and 10 normal non-diabetic subjects. The Charcot arthropathy patients demonstrated a preservation of warm perception, 6 (5.5) °C, but complete loss of peripheral cold perception, 10 (0) °C, p〈0.001 (median (interquartile range)). This contrasted with the ulcerated neuropathy patients, who had equally severe impairment of both warm and cold sensory thresholds, 10 (0.5) °C vs 10 (1) °C, respectively, the diabetic control subjects who were able to detect a 2 (1.3) °C warm stimulus and 3 (3.5) °C cold stimulus and the normal subjects, whose warm threshold was 2 (1) °C and cold was 2 (1) °C. Light touch perception at the foot was preserved in the Charcot patients 4 (4) g vs 100 (50) g, p〈0.0002, in the ulcerated neuropathy patients. Vibration perception at the great toe and cardiovascular autonomic function tests (heart rate variability, Valsalva ratio and postural systolic blood pressure fall) were abnormal in both the Charcot patients and ulcerated neuropathy group, with no differences seen between the two groups. Peak skin blood flow at the great toe in response to local heating was preserved in the Charcot arthropathy patients, 63.36 (28.72) flow units when compared to the diabetic and normal subjects, 62.72 (47) flow units and 76.3 (33.92) flow units, respectively and much greater than in the ulcerated neuropathy patients 28.94 (37.39) flow units, p〈0.0002. The diabetic patients developing Charcot arthropathy thus have a neuropathy and vascular responsiveness which distinguishes them from diabetic subjects developing neuropathic ulceration. This may be important in the pathogenesis of the Charcot foot.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00402547
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    HUMAN VASCULAR α-ADRENOCEPTORS: THE RELEVANCE OF SUBTYPES (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 14 (1987), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY1. The post-receptor mechanisms of α1 and α2-adrenoceptor subtypes in guinea-pig aorta and human digital arteries have been explored.2. Nifedipine antagonized contractile responses of human digital arteries to TL99 and methoxamine to a similar degree, thus suggesting that neither the α1 nor the α2 receptor is preferentially linked to calcium entry through voltage-operated channels of the cell membrane.3. In the guinea-pig aorta, which contains only α1-adrenoceptors, methoxamine-stimulated inositol phosphate (IP) production at similar concentrations was required to produce contractile responses.4. In the human digital artery, noradrenaline also produced a significant increase in IP formation, but preliminary experiments have suggested that both TL99 and methoxamine stimulate IP production.5. Thus, the present authors have been unable as yet to confirm, in a tissue which contains both α1-and α2-adrenoceptors, that the post-receptor mechanisms of the α subtypes are different.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1987.tb00987.x
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  • 5
    Electronic Resource
    Electronic Resource
    ARE NEURONAL UPTAKE MECHANISMS RESPONSIBLE FOR THE DIFFERENCE IN SENSITIVITY TO NORADRENALINE BETWEEN HUMAN ARTERIES AND VEINS? (1980)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 7 (1980), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The sensitivity of human metacarpal veins and digital arteries obtained post-mortem to noradrenaline and phenylephrine has been tested.2. pED50 values for noradrenaline were significantly higher in the veins (699, s.e.m. = 008) than in the arteries (6.56, s.e.m. = 009), whereas pED50 values for phenylephrine in the two tissues were not significantly different (arteries: 6.24, s.e.m. = 009; veins: 6.26, s.e.m. = 005).3. The addition of propranolol (4 × 10−6 mol/l) alone, or in combination with hydrocortisone (4 × 10−5 mol/l), did not affect the responses to either noradrenaline or phenylephrine. The further addition of cocaine (3 × 10−5 mol/l) slightly shifted the noradrenaline and phenylephrine concentration-effect curves to the left in both arteries and veins, but veins were still found to be more sensitive than arteries to noradrenaline whilst there was still no difference in the sensitivity of veins and arteries to phenylephrine.4. Cocaine also slightly potentiated responses to barium chloride, potassium chloride and serotonin.5. It is concluded that the difference in sensitivity to noradrenaline between arteries and veins cannot be explained by differences in neuronal uptake and it is possible that there may be differences in the properties of the postsynaptic α-adrenoreceptors of the two tissues. It is also concluded that the potentiation of the contractile effect of noradrenaline produced by cocaine is not solely due to inhibition of neuronal uptake of amines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1980.tb00055.x
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    Paper (German National Licenses)
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